Low concentration of lipopolysaccharide acts on MC3T3‐E1 osteoblasts and induces proliferation via the COX‐2‐independent NFκB pathway
Low concentration of lipopolysaccharide acts on MC3T3‐E1 osteoblasts and induces proliferation via the COX‐2‐independent NFκB pathway
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DOI：
10.1002/cbf.1563
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发表时间：
2009-06
影响因子：
3.6
通讯作者：
Leyu Wang;Hai-yi Wang;Jun Ouyang;Lei Yu;Bing Chen;Jian-qiang Qin;Xiao-zhong Qiu
中科院分区：
文献类型：
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作者：
Leyu Wang;Hai-yi Wang;Jun Ouyang;Lei Yu;Bing Chen;Jian-qiang Qin;Xiao-zhong Qiu
在骨折过程中，肠道内脂多糖（LPS）的移位及其对骨愈合的影响通常是临床感兴趣的。环氧合酶-2（Cyclooxygenase-2，考克斯-2）是前列腺素E2（prostaglandin E2，PGE 2）产生的关键酶，能诱导核因子κ B（nuclear factor kappa B，NFκB）活化，促进骨折愈合。为了了解它们在骨骼再生中的作用，在LPS存在的情况下，用NFκB抑制剂BAY 11 - 7082和sc 791（一种选择性考克斯-2抑制剂）处理小鼠MC 3 T3-E1成骨细胞。有趣的是，LPS可通过增加NFκB B的活化和转位来诱导成骨细胞增殖。这种诱导与考克斯-2表达无关，表明LPS诱导的NFκB活化不依赖于考克斯-2。低浓度的LPS可能作为NFκB B通路的刺激因子在未受刺激的细胞如成骨细胞中起作用。考克斯-2对于LPS诱导的成骨细胞增殖过程中的NFκB通路不是必需的，因为sc 791对这种诱导没有影响。这些研究提供了一个潜在的机制，LPS可以影响骨组织修复在炎症的初始阶段的洞察。版权所有© 2009约翰威利父子有限公司。
The translocations of lipopolysaccharide (LPS) from the gut and its effects on bone healing are usually of clinical interest during bone fracture. As already widely stuided, Cyclooxygenase‐2 (COX‐2) is a key enzyme for prostaglandin E2 (PGE2) production, which induces the nuclear factor kappa B (NFκB) activation and is beneficial to fracture healing. In order to know their roles in skeletal regeneration, mouse MC3T3‐E1 osteoblasts were treated with NFκB inhibitor BAY 11‐7082 and sc791 (a selective COX‐2 inhibitor), in the presence of LPS. Interestingly, LPS could induce osteoblasts proliferation through increasing NFκB activation and translocation. This induction was not related to COX‐2 expression, suggesting that LPS‐induced NFκB activiation is independent of COX‐2. It is possible that low concentration of LPS can act as a stimulating factor of the NFκB pathway in nonstimulated cells such as osteoblasts. COX‐2 is not necessary for the NFκB pathway during LPS‐induced proliferation of osteoblasts since sc791 had no effects on this induction. These studies provide insight into a potential mechanism by which LPS can affect bone tissue repair in the initial phase of inflammation. Copyright © 2009 John Wiley & Sons, Ltd.